[unreadable] The respiratory epithelium plays a pathogenic role in airway and lung disease by regulating mucosal inflammation and tissue fibrosis. Sarcoidosis is associated with epithelial activation and mucosal inflammation. Granuloma formation is typically bronchocentric and certain cytokines such as osteopontin, interferon gamma and interleukin-4 are up-regulated in sarcoid epithelial cells. This is perhaps not surprising as the portal of entry of relevant sarcoidosis antigen(s) is likely to be via the respiratory mucosal route. In sarcoid patients respiratory mucosal involvement manifests clinically as airway obstruction and nasal congestion and has been associated with recalcitrant and progressive disease. Epithelial and respiratory mucosal manifestations of sarcoidosis are more common in African Americans, a group of patients that have disproportionately more morbidity and mortality from sarcoidosis. Despite these data the role of the respiratory epithelium in regulating sarcoidal inflammation and fibrosis has not been studied. We hypothesize that respiratory epithelial and mucosal responses in sarcoidosis may influence disease pathogenesis by releasing mediators which regulate the influx and maturation of mucosal inflammatory cells and ultimately tissue fibrosis. We believe that the nasal epithelium provides an ideal approach to study these hypotheses because there is a high prevalence of nasal symptoms in sarcoidosis, the fact that nasal mucosal responses have provided interesting insights into other diseases yet represent a novel approach to sarcoidosis, and nasal studies are safe and feasible with a high likelihood for longitudinal follow up studies. We propose to characterize the prevalence, etiology and immuno-pathology of nasal disease in this population by recruiting a cohort of sarcoid patients from the Sarcoidosis Clinic at Boston Medical Center. Results will be correlated with sarcoid disease phenotype. We believe that these studies will challenge the current hypothesis that sarcoidosis is exclusively a Th1 mediated disease and may provide novel avenues to classify sarcoidosis based on nasal mucosal responses. Furthermore this work should provide the basis for additional studies pertaining to sarcoidosis. (End of Abstract) [unreadable] [unreadable]